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From Revolution to Evolution: The Glutamate Hypothesis of Schizophrenia and its Implication for Treatment
by
Moghaddam, Bita
, Javitt, Daniel
in
Adult and adolescent clinical studies
/ Alzheimer's disease
/ Antipsychotics
/ Biological and medical sciences
/ Cognition & reasoning
/ Dopamine
/ Glutamic Acid - physiology
/ Humans
/ Hypotheses
/ Ketamine
/ Medical sciences
/ Neuropharmacology
/ Neuropsychopharmacology Reviews
/ Neurosciences
/ Neurotransmitter Agents - physiology
/ Pharmaceutical industry
/ Pharmacology. Drug treatments
/ Psychiatry
/ Psycholeptics: tranquillizer, neuroleptic
/ Psychology. Psychoanalysis. Psychiatry
/ Psychopathology. Psychiatry
/ Psychopharmacology
/ Psychoses
/ Psychosis
/ Psychotropic drugs
/ Psychotropic Drugs - therapeutic use
/ Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors
/ Receptors, N-Methyl-D-Aspartate - physiology
/ Schizophrenia
/ Schizophrenia - drug therapy
/ Schizophrenia - metabolism
/ Schizophrenia - physiopathology
2012
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From Revolution to Evolution: The Glutamate Hypothesis of Schizophrenia and its Implication for Treatment
by
Moghaddam, Bita
, Javitt, Daniel
in
Adult and adolescent clinical studies
/ Alzheimer's disease
/ Antipsychotics
/ Biological and medical sciences
/ Cognition & reasoning
/ Dopamine
/ Glutamic Acid - physiology
/ Humans
/ Hypotheses
/ Ketamine
/ Medical sciences
/ Neuropharmacology
/ Neuropsychopharmacology Reviews
/ Neurosciences
/ Neurotransmitter Agents - physiology
/ Pharmaceutical industry
/ Pharmacology. Drug treatments
/ Psychiatry
/ Psycholeptics: tranquillizer, neuroleptic
/ Psychology. Psychoanalysis. Psychiatry
/ Psychopathology. Psychiatry
/ Psychopharmacology
/ Psychoses
/ Psychosis
/ Psychotropic drugs
/ Psychotropic Drugs - therapeutic use
/ Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors
/ Receptors, N-Methyl-D-Aspartate - physiology
/ Schizophrenia
/ Schizophrenia - drug therapy
/ Schizophrenia - metabolism
/ Schizophrenia - physiopathology
2012
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Do you wish to request the book?
From Revolution to Evolution: The Glutamate Hypothesis of Schizophrenia and its Implication for Treatment
by
Moghaddam, Bita
, Javitt, Daniel
in
Adult and adolescent clinical studies
/ Alzheimer's disease
/ Antipsychotics
/ Biological and medical sciences
/ Cognition & reasoning
/ Dopamine
/ Glutamic Acid - physiology
/ Humans
/ Hypotheses
/ Ketamine
/ Medical sciences
/ Neuropharmacology
/ Neuropsychopharmacology Reviews
/ Neurosciences
/ Neurotransmitter Agents - physiology
/ Pharmaceutical industry
/ Pharmacology. Drug treatments
/ Psychiatry
/ Psycholeptics: tranquillizer, neuroleptic
/ Psychology. Psychoanalysis. Psychiatry
/ Psychopathology. Psychiatry
/ Psychopharmacology
/ Psychoses
/ Psychosis
/ Psychotropic drugs
/ Psychotropic Drugs - therapeutic use
/ Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors
/ Receptors, N-Methyl-D-Aspartate - physiology
/ Schizophrenia
/ Schizophrenia - drug therapy
/ Schizophrenia - metabolism
/ Schizophrenia - physiopathology
2012
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From Revolution to Evolution: The Glutamate Hypothesis of Schizophrenia and its Implication for Treatment
Journal Article
From Revolution to Evolution: The Glutamate Hypothesis of Schizophrenia and its Implication for Treatment
2012
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Overview
Glutamate is the primary excitatory neurotransmitter in mammalian brain. Disturbances in glutamate-mediated neurotransmission have been increasingly documented in a range of neuropsychiatric disorders including schizophrenia, substance abuse, mood disorders, Alzheimer's disease, and autism-spectrum disorders. Glutamatergic theories of schizophrenia are based on the ability of N-methyl-D-aspartate receptor (NMDAR) antagonists to induce schizophrenia-like symptoms, as well as emergent literature documenting disturbances of NMDAR-related gene expression and metabolic pathways in schizophrenia. Research over the past two decades has highlighted promising new targets for drug development based on potential pre- and postsynaptic, and glial mechanisms leading to NMDAR dysfunction. Reduced NMDAR activity on inhibitory neurons leads to disinhibition of glutamate neurons increasing synaptic activity of glutamate, especially in the prefrontal cortex. Based on this mechanism, normalizing excess glutamate levels by metabotropic glutamate group 2/3 receptor agonists has led to potential identification of the first non-monoaminergic target with comparable efficacy as conventional antipsychotic drugs for treating positive and negative symptoms of schizophrenia. In addition, NMDAR has intrinsic modulatory sites that are active targets for drug development, several of which show promise in preclinical/early clinical trials targeting both symptoms and cognition. To date, most studies have been done with orthosteric agonists and/or antagonists at specific sites. However, allosteric modulators, both positive and negative, may offer superior efficacy with less danger of downregulation.
Publisher
Nature Publishing Group
Subject
Adult and adolescent clinical studies
/ Biological and medical sciences
/ Dopamine
/ Humans
/ Ketamine
/ Neuropsychopharmacology Reviews
/ Neurotransmitter Agents - physiology
/ Pharmacology. Drug treatments
/ Psycholeptics: tranquillizer, neuroleptic
/ Psychology. Psychoanalysis. Psychiatry
/ Psychotropic Drugs - therapeutic use
/ Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors
/ Receptors, N-Methyl-D-Aspartate - physiology
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